ArticleJournal of thoracic disease2018
The role of NF-κB-mediated JNK pathway in cognitive impairment in a rat model of sleep apnea.
Article in Journal of thoracic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Cerebral oxidative stress, inflammation and apoptosis induced by intermittent hypoxia: a systematic review and meta-analysis of rodent data.European respiratory review : an official journal of the European Respiratory Society · 2024Pooled it
- Quantitative and morphological analyses reveal microglia-specific neuroinflammation in brain regions linked to cognitive function in ovariectomized and chronic intermittent hypoxia-exposed female rats.Brain, behavior, & immunity - health · 2026Article
- Echinocystic Acid Antagonizes Post-Stroke Depression in Mice by Suppressing the JNK/NF-κB Signaling Pathway.Neuropsychiatric disease and treatment · 2026Article
- Brain nitric oxide and inflammation in chronic intermittent hypoxia: Contributors to cognitive impairment and hypertension.Brain, behavior, & immunity - health · 2025Review
- The role of melatonin in affecting cognitive dysfunction in acute sleep deprivation mice through the nuclear factor kappaB pathway and oxidative stress.Translational neuroscience · 2025Article
- Unraveling the Complexities of Oxidative Stress and Inflammation Biomarkers in Obstructive Sleep Apnea Syndrome: A Comprehensive Review.Life (Basel, Switzerland) · 2024Review
- The common link between sleep apnea syndrome and osteoarthritis: a literature review.Frontiers in medicine · 2024Review
- Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome.Signal transduction and targeted therapy · 2023Review
- Apnea of prematurity induces short and long-term development-related transcriptional changes in the murine cerebellum.Current research in neurobiology · 2023Article
- Active metabolites and potential mechanisms ofFrontiers in pharmacology · 2023Article
- Treatment of Modified Dahuang Fuzi Decoction on Cognitive Impairment Induced by Chronic Kidney Disease through Regulating AhR/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Expression of TLR2 and TLR5 in distal ileum of mice with obstructive jaundice and their role in intestinal mucosal injury.Archives of medical science : AMS · 2022Article
- Repeated neonatal sevoflurane induced neurocognitive impairment through NF-κB-mediated pyroptosis.Journal of neuroinflammation · 2021Article
- The dorsal and the ventral side of hypoglossal motor nucleus showed different response to chronic intermittent hypoxia in rats.Sleep & breathing = Schlaf & Atmung · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of this study is to determine the role of nuclear factor kappa B (NF-κB)-mediated c-Jun N-terminal kinase (JNK) pathway in cognitive impairment induced by chronic intermittent hypoxia (CIH).
methodsNinety-six male Sprague-Dawley rats were randomly divided into 8 groups: sham group, sustained hypoxia (SH) group, CIH group, CIH + melatonin group, CIH + vitamin E group, CIH + DMSO group, CIH + BAY 11-7082 group and CIH + normal saline (NS) group. Rats were exposed to normoxia, CIH (21% O
resultsCompared with the Sham and SH group, oxidative stress was induced by CIH in rat hippocampus with the high level of malondialdehyde (MDA) and 8-iso-PGF2α and the low level of superoxide dismutase (SOD) and glutathione (GSH). Activated NF-κB and its downstream products including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) were highly expressed in CIH rats. These changes were attenuated by pretreatment of the rats with melatonin and vitamin E. CIH also resulted in hippocampus neuron apoptosis with increased caspase 3 level, dUIP nick end labeling (TUNEL)-positive neurons number and cognitive impairment verified by prolonged latency and shortened time in the target quadrant in Morris water maze test. JNK and its downstream transcriptional factors including c-Jun, activating transcription factor 2 (ATF2), and JunD were all significantly phosphorylated in CIH rats. However, pretreatment of NF-κB inhibitor BAY 11-7082 inhibited the activation of NF-κB under CIH condition and also significantly reduced the phosphorylation of JNK as well as c-Jun, ATF2, and JunD. Moreover, hippocampus neuron apoptosis and cognitive impairment were significantly improved with the pretreatment of BAY 11-7082 in rats subjected to CIH.
conclusionsThese findings suggest that NF-κB-mediated JNK pathway is at least partially implicated in CIH-induced hippocampus neuron apoptosis and cognitive impairment. Inhibition of NF-κB activation provided a therapeutic potential for cognitive impairment in sleep apnea (SA).
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